Naturally conducted or intrinsic ventricular depolarizations have been recognized as being preferable over ventricular pacing in general and pacing in the right ventricular apex in particular. In order to minimize or greatly reduce ventricular pacing, protocols have been developed that, in general, utilize an atrial based timing mode that promotes intrinsic conduction whenever possible. Illustrative protocols are described in U.S. Pat. No. 7,218,965 (Casavant), U.S. Pat. No. 6,772,005 (Casavant), and U.S. Pat. No. 7,248,924 (Casavant), all of which are incorporated herein by reference in their entireties.
Atrial based pacing in general, as well as in the context of minimizing ventricular pacing as discussed above, may also include a rate response function. As a metabolic demand sensor indicates a need for increased cardiac output, the heart rate is elevated by increasing the atrial pacing rate. However, without ventricular pacing, there is no control over the ventricular timing. As such, if the intrinsically conducted ventricular event results in an atrial to ventricular delay (AV delay) that is not shortened, or is actually elongated by the AV node in response to the elevated pacing rate, overall timing of the cardiac chamber contractions may become skewed. That is, the A-A interval is decreasing but the AV delay is not correspondingly and correctly modified. As a consequence, VA delay (ventricular to atrial interval) may be shortened. Another consequence may be Wenckebach block in which given ratios of ventricular beats are not conducted with respect to the atrial rate. As such, even though the atrial rate may rise, the effective ventricular rate could actually decrease.
If the VA delay becomes too short over a prolonged period of time, negative consequences may result. The contraction of the ventricles takes a finite amount of time from initiation of a depolarization. If the contraction is not completed, a subsequent atrial contraction will attempt to force blood into a contracted ventricle, against a closed valve. Often, this results in retrograde blood flow out of the atria and back toward the lungs and venous system, which can become symptomatic. Similarly, the ventricles even if not fully contracted may not be fully relaxed during the atrial contraction, resulting in diminished filling. The net effect of having inadequate VA delay is that the elevation in heart rate fails to increase cardiac output, may actually reduce cardiac output, may result in hemodynamic compromise, and/or cause adverse patient symptoms.